During our life moving, walking, sport, etc. is essential for our health and quality of life. We fully depend on joint motion for these abilities. The presence of healthy articular cartilage is essential for joint motion. Articular cartilage is exposed to an enormous amount of intensive and repetitive forces during life. The wear resistance and friction modus of articular cartilage are unique, however when damaged, cartilage has a limited capacity for regeneration. Articular cartilage lesions which fail to heal spontaneously eventually evolve in osteoarthritis (OA)3, 6, 7.
OA is among the most frequent forms of musculoskeletal disorders affecting over 10% of the adult population9. While primary osteoarthritis (OA) is defined as joint degeneration without any underlying cause, in secondary OA joint degeneration is often caused by trauma (e.g. during sports or in traffic accidents). Traumatic cartilage lesions can be asymptomatic, the percentage of individuals suffering from OA due to a trauma is unknown and may be underestimated. From literature it is known that sixteen to twenty percent of patients with a traumatic hemarthros have a cartilage defect4, 8, and even up to 60% of patients undergoing a arthroscopy have a cartilage defect1, 2, 5. OA is a significant socio-economic burden and recent developments for treatment of OA have led to an increasing interest for this affection. Together with rheumatoid arthritis (RA) OA is the most common cause of articular cartilage degeneration.
Many factors have been described to influence cartilage repair and prevent cartilage degeneration. A growing number offers a number of bioactive reagents, including pharmaceutically active agents, proteins (e.g. growth factors) and nucleic acids and can be administered and targeted as such or by using gene-transfer approaches and RNAi,
US 2008269762 A1 relates to a method for treating a cartilage defect in a human subject comprising the steps of obtaining blood compatible with the subject, fractionating said blood to produce platelet-poor plasma, concentrating said platelet-poor plasma to produce a platelet-poor plasma concentrate and administering said concentrate to the site of said cartilage defect.
US 2008274157 A1 describes a method of placing a preshaped allograft implant assembly in a cartilage defect, said assembly comprising a subchondral bone and an overlying cartilage cap plug which has been treated to remove cellular debris and proteoglycans and minced cartilage in a carrier comprising the steps of: (a) drilling a cylindrical hole in a patient at a site of a cartilage defect to a depth which equal to or less than the length of the bone and cartilage cap plug implant to be placed therein forming a blind bore; (b) placing a preshaped osteochondral plug having a cross section which is less than the cross sectional area of the bore with a gap between the exterior surface of the plug and at least one side wall defining the drilled bore being less than 2 mm allowing the implant to be laterally moveable within said bore in the cylindrical hole; (c) mixing minced allograft cartilage in a fibrinogen thrombin solution; and (d) placing the minced cartilage in fibrinogen thrombin solution in the gap between the plug and at least one side wall defining the bore and allowing the cartilage and solution to polymerize.
US 2008269895 A1 is concerned with an implant suitable for the repair of a cartilage defect in a human or animal subject, which implant comprises an implant body including a natural cartilage matrix produced by in vitro tissue culturing from cells or produced from ex vivo cartilage tissue and which implant further comprises viable cells having a chondrogenic potential and adhered to the surface of the implant body.
Jean et al. (OsteoArthritis and Cartillage (2007) 15, 638-645) describes the effect of intra-articular injection of the cyclooxygenase-2 (COX-2) inhibitor parecoxib on osteoarthritis (OA) progression. Parecoxib alone did not have any effect on cartilage and synovium of normal knees in naive rats. In anterior cruciate ligament-transected (ACLT) knees, parecoxib showed significant inhibition of cartillage degeneration. Intra-articular parecoxib injection suppressed synovial inflammation, and glutamate and aspartate levels were reduced as well. This shows that intra-articular injection of a COX-2 inhibitor inhibits ACLT-induced OA progression.
US 2008262618 A1 provides a prosthesis device, comprising: a body at least partly formed from a segmented thermoplastic elastomer having crystallized blocks, and having at least one functional component which is able to reversibly bond to the crystallized blocks, wherein the elastomer has cartilage regenerative properties.
WO 2008122595 A2 relates to an at least partially biodegradable implant suitable for implantation into a subject for repairing a bone or cartilage defect, comprising: a matrix of a non-particulate material, the matrix having an open-celled structure having a plurality of interconnected spaces, and a plurality of particles of a metallic material, wherein the spaces in the matrix are substantially completely filled with the metallic material particles, and wherein at least one of the metallic material or the matrix material is at least partially degradable in-vivo.
EP 1932536 A2 discloses a collagenase composition for the treatment of soft tissue, wherein the treatment comprises applying the collagenase composition to a defect or injury in soft tissue in a patient, thereby promoting healing of the defect or injury.